Mechanistic studies using heterotypic co-cultures of normal and cancerous urothelial cells with normal and tumor associated stromal cells indicated that SPARC inhibited the acquisition inflammatory secretory phenotype of tumor associated macrophages (TAMs) and cancer associated fibroblasts (CAFs) through inhibition of the activation of NFκB and AP-1 with subsequent decrease in their secreted cytokines and cancer cell invasiveness. The gene discussed is NFKB1; the disease is neoplasm.